Hyperuricemia is the cause of urate deposition diseases including gouty arthritis and renal disorder (NPL 1). The prevalence of hyperuricemia in Japan has been reported as 21.5% in adult males. The prevalence in adult males by age is highest in the 30s and 40s, and approximately reaches 30% (NPL 2). Meanwhile, it has been known that the serum uric acid level increases post menopause, and the prevalence of hyperuricemia in females is reported as 1.3% and 3.7% in those under and over 50 years old, respectively. The results suggest that the incidence of this disease is high in men. The number of gout patients tends to be increasing year by year (NPL 3) and the number of patients with asymptomatic hyperuricemia, as the potential patients, has been estimated as 8,000,000 in Japan.
In the past, hyperuricemia has been attracting attention as the cause of urate deposition diseases such as gout arthritis, gouty tophus, and urinary calculus as described above. However, in recent years, the clinical report that overturns this concept, in other words, a possibility of suggesting that uric acid itself regardless of deposition is deeply involved in onset and progression of chronic kidney disease, cardiovascular disease, and metabolic syndrome as a causative factor has been reported (NPL 4). Further, allopurinol serving as a therapeutic agent of hyperuricemia not only decrease the uric acid level, it has also shown the possibility that allopurinol suppresses cardiovascular disorders such as hypertension, ischemic disease, and heart failure (NPL 5).
Control of the serum uric acid level is involved in re-absorption and secretion of uric acid in the proximal tubule of the kidney (NPL 6). In the re-absorption of uric acid, Urate Transporter 1 (URAT1) existing in the proximal tubule plays an important role (NPL 7). URAT1 is an organic anion transporter-like molecule identified from both of gene database analysis and expression function analysis using oocytes (NPL 7). URAT1 was identified on the brush border membrane side of the proximal tubular epithelial cells as 12-transmembrane protein and shown to transport uric acid by exchanging with a chloride ion or organic anions. Since lactic acid and pyrazine carboxylic acid serving as an uricosuric agent promote activity of URAT1, the re-absorption of uric acid in the kidney is promoted (NPL 9). On the other hand, URAT1 is inhibited by benzbromarone, probenecid, and losartan. In some patients with renal hypouricemia, it has been reported that the function of re-absorbing uric acid in the kidney is significantly degraded due to mutations of URAT1 and the serum uric acid level is low (NPL 9). Therefore, since the inhibition of URAT1 decreases the serum uric acid level, probenecid or benzbromarone has been used as a therapeutic agent of hyperuricemia.
Hyperuricemia has been largely classified into three types, such as a uric acid overproduction type, a uric acid underexcretion type, and a combined type. Among them, the number of patients is the highest in underexcretion type and an uricosuric agent such as probenecid or benzbromarone is selected as a therapeutic agent for these patients (NPL 1). Further, hyperuricemia with complications of lifestyle related diseases is mainly uric acid underexcretion type and re-absorption of uric acid in the proximal tubule of the kidney is believed to be a factor of the onset of hyperuricemia (NPL 8). Therefore, it makes sense to treat hyperuricemia patients having complications of lifestyle related diseases using a drug which inhibits re-absorption of uric acid in the kidney and promotes excretion of uric acid. However, probenecid is a drug which is highly interactive with drugs so that probenecid is required to be cautious when used in combination and it is known that the effects of probenecid is significantly decreased when it is used for hyperuricemia patients having complications of renal disorder (NPL 1). Meanwhile, benzbromarone is considered to be effective for hyperuricemia patients with somewhat reduced kidney functions, but it is reported that benzbromarone causes severe side effects such as fulminant hepatitis (NPL 1). For this reason, in overseas there are some countries that prohibit the use of benzbromarone. Accordingly, a highly safe URAT1 inhibitor is expected to be widely used, as the best-in-class, for the most common hyperuricemia patients having uric acid underexcretion type.

Further, recently, PTLs 1 and 2 describe that a naphthyl-substituted triazole thioacetate derivative or pyridyl thioacetate derivative represented by Formula (A) or (B) exhibits excellent hURAT1 inhibitory actions in uric acid uptake assays using a hURAT1 transporter and thus is useful as a therapeutic agent for hyperuricemia.

Further, PTL 3 describes that a benzbromarone derivative represented by Formula (C) exhibits hURAT1 inhibitory activity, is not interactive between drugs with respect to cytochrome P450 (CYP450), exhibits selectivity between organic anion transporters, and thus has higher solubility and metabolic stability.
The compound represented by the following Formula (I) and the compound represented by Formula (A) or (B) are different from each other in terms that a ring to which thioalkanoic acid is bonded is a bicyclic compound in the former one and a ring to which thioalkanoic acid is bonded is monocyclic in the latter one.
Further, the compound represented by the following Formula (I) and the benzbromarone derivative represented by Formula (C) are clearly different from each other in terms of a structure.
On the other hand, PTL 4 and NPLs 10 and 11 describe compounds represented by the following Formulae (D), (E), and (F) as examples of compounds in which a quinoline ring or a naphthalene ring is substituted with a phenyl group, thioalkanoic acid, or oxyalkanoic acid.

On the other hand, NPLs 12 and 13 describe compounds represented by the following Formulae (G) and (H) as examples of compounds which have a 1,1′-binaphthalene structure and in which a 2-position of naphthalene has oxyacetic acid and the other 2′-position is substituted with a hydroxy group or a methoxy group.

However, in NPLs 12 and 13, there is no description that any of the compounds represented by Formulae (D) to (H) has a hURAT1 inhibitory action.